Criado por Jessica Margaux Mercado
aproximadamente 9 anos atrás
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Impaired cardiac function → unable for the cardiac muscles to contract → unable to propel the blood to the systemic circulation → unable to supply oxygen to metabolic processes
Pathophysiologic state resulting from impaired cardiac function that renders the heart muscle unable to maintain an output sufficient for the metabolic requirements of the tissues & organs
In order to maintain the CO, the heart muscles must stretch → dilatation of the heart muscles → increase in the preload and increase in the contractility of the heart → increased cardiac output (volume pumped out).
Increased cross-sectional areas of the myocytes; increase wall thickness , reduced cavity diameter
deposition of new sarcomeres;
cell length and width and muscle mass and wall thickness are increased in proportion to chamber diameter
CHF: Fetal gene program
Mechanism: direct impairment of myocardial contractility
(CHF)
Mechanism: excessive pressure
(CHF)
Mechanism: excessive volume
(CHF)
Mechanism: high output states
(CHF)
Mechanism: reduced myocardial expansion
(CHF)
Mechanism: disrupted electrical function
(CHF)
Mechanism: unknown
(CHF)
Mechanism: electrical conduction disruption
(CHF)
Mechanism: Inflammation, Degenerative, Congenital
(CHF)
Mechanism: Congenital
(CHF)
CHF: Impaired contractile function → dec CO;
S/S: pulmonary congestion;
progressive deterioration of myocardial contractile function
CHF: reduced ventricular compliance;
Inability of the heart to relax and expand → dec ventricular filling → dec CO
Left-Sided Heart Diseases
Pulmonary congestion, edema;
Peripheral edema, hypoxic encephalopathy
dyspnea, exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea , tachy, cardiomegaly, blood-tinged sputum, cyanosis, rales
Causes: pulmonary embolism, intrinsic lung disease (COPD, cystic fibrosis), pulmonary HPN, kyphoscoliosis, pneumoconiosis, schistosomiasis
Mechanism: Increased pulmonary vascular resistance due to fibrosis and/or hypoxic vascular response
CPC of liver, centrilobular necrosis, sclerosis; congestive splenomegaly, congestion in kidneys, hypoxic encephalopathy, ascites, pleural effusion, edema
splanchnic congestion: hepato-splenomegaly, hepatojugular reflex, jugular venous distention, dependent edema, transudative effusions (ascites, pleural effusion), cyanosis
heart failure secondary to pumping excessive volume of blood
High-Output Failure: causes
Secondary to ischemic heart disease (IHD), hypertension, dilated cardiomyopathy, and vulvar/pericardial disease
CRITERIA FOR DX OF CHF: Major Criteria
CRITERIA FOR DX OF CHF: Minor Criteria
imbalance between blood supply/perfusion to the heart and its demand for oxygenated blood; limits oxygenation, ATP generation, reduces availability of nutrients and removal of metabolic wastes
Syndromes: AMI, angina pectoris, chronic ischemic heart disease, sudden cardiac death
dec coronary artery perfusion relative to myocardial demand; chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries, variable degrees of superimposed acute plaque change, thrombosis, and vasospasm
70% of lumen of one or more CA is/are obstructed with atherosclerotic plaque; compensatory CA vasodilatation is insufficient to meet moderate increases in myocardial O2 demand
acute plaque changes
myocardial infarct where the whole wall of the muscle has undergone cell death
Paroxysmal, recurrent precordial or substernal chest pain, caused by transient (15s to 15min) myocardial ischemia that falls short of infarction
chest pain: transient (<15 min), precipitated by exertion and emotion, relieved by rest, vasodilators
Episodic, recurrent chest pain at rest; caused by coronary artery spasm; ECG: suggestive of transmural ischemia (ST segment elevation); responds promptly to vasodilators
90% vessel block; pain progressiveljy increasing in frequency, duration (>15 min), intensity, occurs at rest
local coagulative necrosis of myocardium due to ischemia; irreversible damage to myocardium
Severe Ischemia 20-40 mins. or longer + <10% blood flow + initial damage to sarcolemma membrane
Pathognomonic sign: ischemic coagulative necrosis; central damage at subendocardium progresses into transmural in a waveform fashion
involves >2/3 or full thickness of ventricular wall; ischemia due to superimposed thrombus in atherosclerosis (chronic obstruction + acute plaque change + complete thrombosis)
inner 1/3 or 1/2 of ventricular wall; ischemia due to dec blood volume (e.g. hypovolemic shock, hypotension, diffuse stenosing coronary artery atherosclerosis w/o thrombosis and acute plaque change)
triphenyl tetrazolium chloride: unstained pale zone (due to the lactate dehydrogenase leakage that follows cell death)
S/S: hypotension, rapid weak pulse, diaphoretic & nauseous, dyspnea; ECG: ST elevation, new Q waves, T wave inversion
progressive heart failure as a consequence of ischemic myocardial damage → fibrosis → reduce cardiac activity → ischemia
Gross: left ventricular dilation and hypertrophy, often with discrete areas of gray-white scarring; moderate to severe atherosclerosis;
Histo: diffuse subendocardial myocyte vacuolization, fibrosis from previous infarction
SA node damaged → AV node takes over
atrial dilation → irritable atrial myocytes →independent & sporadic depolarization of each atrial myocytes → variable signal transmission to AV node
dysfunctional AV node:
inc PR interval on ECG
dysfunctional AV node:
intermittent signal transmission
dysfunctional AV node:
complete failure
S/S: palpitations, lightheadedness, syncope, sudden cardiac death
adaptive response to pressure overload on the heart that can lead to myocardial dysfunction, cardiac dilatation, CHF and in some cases sudden death
Concentric left ventricular hypertrophy in the absence of other cardiovascular pathology that might induce cardiac hypertrophy
Gross: thickened left ventricular wall (concentric), cardiomegaly, decreased luminal size;
Histo: inc transverse diameter of the myocytes, boxcar nuclei, intercellular fibrosis
pressure overload in the right ventricle due to increased pulmonary resistance usually caused by chronic lung disease that can lead to pulmonary vasculature fibrosis
right ventricular dilatation after massive pulmonary embolization
right ventricular (and often right atrial) hypertrophy; result of chronic RV pressure overload; seen in COPD, CRPD, long standing pulmonary artery disease, chest wall motion impairment
Gross: marked RV dilation without hypertrophy
Gross: RV wall thickens and RV dilation may lead to tricuspid regurgitation
heart disease resulting from a primary abnormality in the myocardium; attributed to intrinsic myocardial disease
biventricular and bi-atrial dilatation; hypo-contracting heart muscle; systolic dysfunction; low LV ejection fraction, low CO = congestion
Causes: idiopathic, previous viral myocarditis, alcohol or other toxic exposure, peripartum cardiomyopathy/pregnancy, genetic causes, iron overload
cardiomegalic heart, global enlargement, generalized chamber dilatation, annular ring dilatation, valvular defects, functional regurgitation, mural thrombus
ages of 20-50, slowly progressive CHF, including dyspnea, easy fatigability, poor exertional capacity; secondary mitral regurgitation and abnormal cardiac rhythms are common, and embolism from intracardiac (mural) thrombi
Idiopathic Hypertrophic Subaortic Stenosis (IHSS), Hypertrophic Obstructive CM, Asymmetric Septal Hypertrophy
myocardial hypertrophy in the interventricular septum w/o ventricular dilatation, abnormal diastolic filling and LV outflow obstruction; heavy, muscular, hypercontracting heart
missense mutation in sarcomere (B-MHC gene); inc myofilament activation = myocyte hypercontractility
Asymmetric septal hypertrophy → outflow obstruction; septal wall ratio >1.3; massive myocardial hypertrophy w/o ventricular dilatation; banana-like ventricular cavity
Impaired diastolic filling of the massively hypertrophied LV; dec CO and increase in pulmonary venous pressure -> exertional dyspnea with harsh systolic ejection murmur
Gross: non-dilated ventricular chamber; bi-atrial dilatation due to poor ventricular filling and pressure overload;
Histo: patchy or diffuse interstitial fibrosis, identifiable depositions/infiltrations
Dense diffuse fibrosis of ventricular endocardium and subendocardium, often involving the tricuspid and mitral that extends from the apex upward; linked to nutritional deficiencies and/or inflammation related to helminthic infections
Hypereosinophilia and eosinophilic tissue infiltrates, endomyocardial fibrosis, large mural thrombosis
Focal or diffuse thickening usually involving the mural LV endocardium; heart is infiltrated by fibroelastic tissue
Inherited disease; defective cell adhesion proteins in desmosomes that link adjacent myocytes; right ventricular failure and rhythm disturbances (particularly ventricular tachycardia or fibrillation) with sudden death
Disorder characterized by arrhythmogenic right ventricular cardiomyopathy and hyperkeratosis of plantar palmar skin surfaces
RV wall: severely thinned because of loss of myocytes, extensive fatty infiltration and fibrosis
infectious agents and/or inflammatory processes primarily target the myocardium; result in injury to cardiac myocytes (necrosis and degeneration) not typical of ischemic heart disease
Gross: beefy red myocardium due to vascular congestion; ventricular myocardium is flabby and mottled by either pale foci or minute hemorrhagic lesions
Histo: interstitial inflammatory myocardial necrosis near the inflammatory cells; vascular congestion, edema; viral inclusions and parasitic organisms may be present
edema, interstitial inflammatory infiltrates, and myocyte injury; diffuse lymphocytic infiltrate; self-limiting
presence of multi-nucleated giant cells; infiltrates: Lymphocytes, eosinophils, necrosis, patchy myocitic necrosis in muscle cell
Interstitial infiltrate: macrophages, a lot of eosinophils with little or no necrosis; no granulomas; associated with adverse drugs effects of methyldopa
ASD, VSD, PDA, AVSD; acyanotic, right ventricular hypertrophy and eventually failure
early cyanosis; hypertrophic osteoarthropathy, polycythemia, paradoxical embolization;
Tetralogy of Fallot, Transposition of Great Vessels, Truncus Arteriosus, Tricuspid Atresia, TAPVR
untreated congenital cardiac defect with intracardiac communication that leads to pulmonary hypertension, reversal of flow, and cyanosis
Basic defect: Abnormal opening at the level of the atrial septum; most common CHD that is asymptomatic until adulthood; S/S may manifest in 3rd decade
90% of ASD ; defect in the fossa ovale
defect occurs (low-lying) near the AV valve; associated with a clefted anterior mitral valve/ abnormal tricuspid valve
Located at the top, near the entrance of SVC; associated with total anomalous pulmonary venous return to the right atriu
Located in the upper portion of the interventricular septum; affects membranous portion
VSD: located below the pulmonary valve
VSD: found in the muscular wall of the interventricular septum
Presence of holes in the atrial and the ventricular level; abnormal development of atrio-ventricular canal; incomplete closure of AV septum and inadequate formation of the tricuspid valve and mitral valve
Failure of fusion of superior and inferior endocardial cushions with the mid portion of the atrial septum and the muscular (trabecular) portion of the ventricular septum
primum atrial septal defect and a cleft in the mitral valve
Defects of both the primum atrial septum and inlet ventricular septum and the presence of a common atrioventricular valve; free communication of all 4 chambers
AVSD: mitral and tricuspid annuli are separate; usually associated with a primum ASD
AVSD: single atrioventricular valve annulus; defect of the inlet ventricular septum
Persistence of communication between the aorta (a high pressure chamber) and the pulmonary artery (a relatively low pressure chamber) via a non-closure of the ductus arteriosus
continuous, harsh murmur: “Machinery murmur”
inability of the great vessel to rotate to its normal location
VSD; subpulmonic stenosis (right ventricular outflow tract obstruction); overriding of the VSD by the aorta; right ventricular hypertrophy
Heart is large and “boot-shaped” as a consequence of right ventricular hypertrophy; proximal aorta is dilated; hypoplastic pulmonary trunk
Hemodynamic consequences: R-to-L shunting, dec pulmonary blood flow, inc aortic volume; polycythemia w/ attendant hyperviscosity and hypertrophic osteoarthropathy
with good APGAR score (pink complexion, without cyanosis); mild pulmonary stenosis; may present with L→R shunt
severe pulmonary stenosis, greater resistance to right ventricular outflow, R→L shunt (blood cannot go to the lungs → cyanotic)
Abnormal formation of the truncal and aortopulmonary septa
ventrico-aterial discordance: aorta from RV, PA from LV; RV Hypertrophy, LV Hypoplasia/Atrophy
failure of separation of truncus arteriosus into aorta and pulmonary artery; single great artery or a single great vessel that receives blood from both ventricles
Complete absence of the development of the tricuspid valve; cyanosis is present virtually from birth; blood cannot flow into the right ventricle
results from unequal division of AV canal; mitral valve is larger than normal and almost always underdevelopment (hypoplasia) of RV
Pulmonary veins do not drain into left atrium, but into left innominate vein or coronary sinus
Results embryologically when the common pulmonary vein fails to develop or becomes atretic; needs PFO or VSD
common pulmonary vein fails to develop or becomes atretic; right atrial and ventricular dilatation, pulmonary trunk dilation , hypoplastic left atrium
Tubular hyperplasia of aortic arch proximal to Patent Ductus Arteriosus (PDA)
Circumferential narrowing of the aortic segment between the left subclavian artery and the ductus arteriosus; leads to the inc of pressure in the pulmonary trunk proximal to the obstruction
Ridge-like coarctation of aorta at the level of or after ligamentum arteriosus; aortic arch and its vessels are dilated and presence of LVH
disparity in the blood pressure of the upper extremities (increased) and of the lower extremities (decreased)
pulmonary artery and valve becomes tight and stenotic; patient presents with a sinus disorder
Narrowing/obstruction of aortic valve at the level of the valve
Narrowing/obstruction of aortic valve below the aorta
Narrowing/obstruction of aortic valve above the aorta
Failure of valve to open completely, impeding forward flow
Failure of valve to close completely, leading to reversal of flow of blood
No anatomic defect in the valve;
dilated cardiomyopathy – the ventricular chambers dilate → annular ring dilates → annular ring cannot close completely → regurgitation of blood from ventricle to atrium
Most often caused by age-related “wear and tear"; involves the aortic valve which becomes obstructed by the calcium deposits at the roof of the valve
Heaped calcified masses within aortic cusps; protrudes into the sinuses of Valsalva, mechanically impeding valve opening; no commissural fusion
Unequal sized bicuspid valve with midline “raphe”; only two valvular leaflets
Calcific nodular deposits in the annular ring; common in elderly women with myxomatous mitral valve, or mitral valve prolapse
Irregular, stony hard nodules behind the mitral valve leaflets; ballooning of the mitral leaflets; affected leaflets are enlarged, redundant, thick, and rubbery; tendinous cords also tend to be elongated, thinned, and occasionally rupture
Thinning of the valve layer known as the fibrosa layer of the valve; middle spongiosa layer expands, owing to increased deposition of myxomatous (mucoid) material
auscultatory finding caused by abrupt tension on the redundant valve leaflets at chordae tendinae as the valve attempts to close
Colonization of heart valves and mural endocardium by microbiologic agents, forming bulky vegetations; most common valves involved are mitral and aortic
Fibrin deposits on injured endothelium; circulating bacteria are trapped by the forming thrombus, infecting the microthrombi (hematogenous seeding)
Highly virulent organism; arises in normal valve; necrotizing, ulcerative and destructive lesions; bulky, friable vegetations; more severe clinical signs and symptoms, higher morbidity
occurs in previously diseased valve; low virulent organism; insidious clinical onset
. Irregular reddish tan vegetations overlie valve cusps;
Fever, weight loss, fatigue, anorexia, changing murmurs, embolic phenomenom: Roth spots, sub-ungal hemorrhages, CVA, embolic infarcts, focal/diffuse GN, abscesses
Sterile vegetations; associated with debilitated patients, carcinoma, sepsis, and cachexia; nondestructive
Valvular damage is not a prerequisite for NBTE; usually found on previously normal valves; hypercoagulable states are the precursor
Small nodules along lines of closure, may be bulky & friable, single or multiple, leaflets often normal; free of inflammation
Associated with SLE; affects MV and TV; sterile, small vegetations located in the under-surface of cords
finely grandular, fibrinous eosinophilic material containing "hematoxylin bodies"; • Intense valvulitis may be present characterized by fibrinoid necrosis of valve
Caused by carcinoid tumors which secrete vasoactive amines; neuroendocrine tumor;
Clinical findings: episodic skin flushing, cramps, nausea, vomiting and diarrhea
Distinctive, glistening white intimal plaque-like endocardial fibrous thickening on the inside surfaces of the cardiac chambers and both TV and PV; tricuspid insufficiency and pulmonic stenosis
Minor Criteria: migratory polyarthritis, carditis, subcutaneous nodules, erythema marginatum, Sydenham's cholera (St. Vitus "Dance")
Minor Criteria: fever, arthralgia, Hx of sore throat, inc anti-steptolysin O, inc acute phase reactants: ESR, CR
Central zone of degenerating, hyper-eosinophilic extracellular matrix infiltrated by lymphocytes, plasma cells, and plump activated macrophages
plump activated macrophages ; pathognomonic for RF
Diffuse inflammation and Aschoff bodies may be found in any of the 3 heart layers
irregular thickenings, usually in the LA; subendocardial fibrosis
Verruccal necrotic vegetations on lines of closure, Aschoff bodies, Anitschkow monocytes, Caterpillar cells, Mac Callum plaques
Latent period (20-30 years) before symptoms appear; Multi-valvular
Fish mouth deformity; commissural fusion of cusps -> stenosis/regurgitation; deformity or "buttonhole" stenosis (typically affecting MV) and regurgitaion
Leaflet thickening, commissural fusion and shortening, and thickening and fusion of the chordae tendinae; fibrosis & subendocardial fibrosis
large and bulky lesions on the valve cusps that can extend onto the chordae
small, warty vegetations along the lines of closure of the valve leaflets
small, bland vegetations usually attached at the line of closure
big and small, up and down (both sides of valve leaflets) vegetations
Most common form of valvular disease in industrialized countries; 20-40 ages, females; MV are enlarged, hooded or floppy; developmental anomaly of connective tissue from a dense collagen to a myxoid tissue
Myxomatous degeneration; where one or more mitral valve leaflets are “floppy” and prolapse into the LA during systole (because of hooding of valve)
Interchondrial ballooning (hooding) of the mitral leaflets, prolapse into the atrium; leaflets are enlarged, redundant, thick and rubbery; tendinous cords: elongated, thinned, or even ruptured and the annulus is dilated
Mid-systolic click (snapping and tensing of everted cusp)
Characteristically produced by non infectious inflammatory diseases; Scanty Inflammation; May or may not cause pericardial serous effusion
Causes of Serious Pericarditis
Composed of serous fluid variably admixed with fibrous exudate
Reflects an active infection caused by microbial invasion; Frank infection leads to systemic symptoms: Spiking fevers and rigors; Organization by scarring is the usual outcome
Exudate composed of blood mixed with fibrinous or suppurative effusion
Most commonly caused by the spread of malignant neoplasm to the pericardial space; In persons with bleeding diathesis; Often follows cardiac surgery
Pericardial involvement occurs by direct spread from TB foci within the tracheobronchial nodes; Common antecedent of fibrocalcific, chronic constrictive pericarditis; Epitheloid granuloma with Langhan’s giant cell surrounded by PMN inflammation
Obliteration of the pericardial sac with adhesion to parietal pericardium that strains cardiac function;
S/S: Sytolic retraction of the rib cage and diaphragm, pulsus paradoxus
organization merely produces plaque-like fibrous thickenings
Obliteration of the pericardial sac with encasement of the heart in a dense, fibrous or fibrocalcific scar that limits diastolic expansion and cardiac output
Extreme cases can resemble plaster mold (concretio cordis); dense enclosing scar, cardiac hypertrophy and dilation cannot occur; S/S: distant or muffled heart sounds, elevated jugular venous pulse, peripheral edema
most common primary cardiac tumor in adults; benign neoplasm from primitive multipotent mesenchymal cells
GNAS1
PRKAR1A
Region of the fossa ovalis (favored site of origin); sessile or pedunculated masses; vary from globular hard masses, mottled with hemorrhage to soft, transluscent, papillary, or villous lesions having gelatinous appearance
most common primary cardiac tumor in children; commonly discovered in the first years of life; most arise from obstruction of a valvular orifice or ventricular chamber
large rounded, or polygonal cells with cytoplasmic glycogen vacuoles
Vacuoles are separated by strands of cytoplasm running from the plasma membrane to the more or less centrally located nucleus
TSC1 and TSC 2 are absent = myocyte growth
often regress spontaneously, they may be considered as hamartomas rather than true neoplasms
inhibits mTOR
Localized, well circumscribed, benign tumors, mature fat cells, occurs in subendocardium, subepicardium, or myocardiuml; most often located in left ventricle, right atrium, or atrial septum
Nonneoplastic deposition of fat in the atrial septum
Lesions include white and brown adipose tissue and small interspersed areas of myocardium
Curious, usually incidental, sea-anemone-like lesions; resembles Lambl excresences that represents remotely organized thrombus on the aortic valves of older individuals